title: Paeoniflorin suppresses vascular damage and the expression of E-selectin and ICAM-1 in a mouse model of cutaneous Arthus reaction.
abstract: Paeoniflorin (PF) extracted from the root of Paeonia lactiflora pall, displays anti-inflammation properties in several animal models. Adhesion molecules are important for the recruitment of leucocyte to the vessel wall and involved in the pathogenesis of various autoimmune and inflammatory diseases. Herein, we investigate the effects of PF on adhesion molecule expression in a mouse model of cutaneous Arthus reaction and cultured human dermal microvascular endothelial cells (HDMECs). We showed that PF significantly ameliorated the immune complex (IC) induced vascular damage, leucocyte infiltrates and adhesion molecules expression. Furthermore, PF markedly blocked tumor necrosis factor-α (TNF-α)-induced E-selectin and intercellular adhesion molecule-1 (ICAM-1) expression in HDMECs at both mRNA and protein levels. PF also suppressed TNF-α-induced adhesion of polymorphonuclear leucocytes (PMNs) to HDMECs. Finally, western blot data revealed that PF can inhibit the phosphorylation of p38, JNK in TNF-α-treated HDMECs. These data suggest that PF, as an anti-inflammatory agent, can downregulate adhesion molecules expression. PF may be a candidate medicine for the treatment of IC-induced inflammatory response.
authors.affiliation: Department of Dermatovenereology, West China Hospital of Sichuan University, Chengdu, Sichuan, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.forename: Zai-Pei
authors.initials: ZP
authors.lastname: Guo
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.forename: Sha
authors.initials: S
authors.lastname: Qin
authors.forename: Na
authors.initials: N
authors.lastname: Cao
authors.forename: Meng-Meng
authors.initials: MM
authors.lastname: Li
authors.forename: Rui-Zhen
authors.initials: RZ
authors.lastname: Jia
authors.forename: Ting-Ting
authors.initials: TT
authors.lastname: Wang
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D000936:Antigen-Antibody Complex / Q000378:metabolism; D001183:Arthus Reaction / Q000188:drug therapy / Q000378:metabolism*; D015551:Autoimmunity; D001565:Benzoates / Q000494:pharmacology*; D001952:Bridged-Ring Compounds / Q000494:pharmacology*; D002448:Cell Adhesion; D002478:Cells, Cultured; D004195:Disease Models, Animal; D019040:E-Selectin / Q000378:metabolism*; D042783:Endothelial Cells / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D005960:Glucosides / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D007962:Leukocytes / Q000166:cytology; D048670:MAP Kinase Kinase 4 / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008833:Microcirculation; D039821:Monoterpenes; D060888:Real-Time Polymerase Chain Reaction; D012867:Skin / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014652:Vascular Diseases / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism; D006027:Glycosides
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000936:Antigen-Antibody Complex; D001565:Benzoates; D001952:Bridged-Ring Compounds; D019040:E-Selectin; D005960:Glucosides; D018799:Intercellular Adhesion Molecule-1; D048670:MAP Kinase Kinase 4; D039821:Monoterpenes; D014409:Tumor Necrosis Factor-alpha; D048051:p38 Mitogen-Activated Protein Kinases; C015423:peoniflorin; D006027:Glycosides